Plus d’anticorps contre CLOCK partenaires d’interaction

In vivo functional characterization of PER O-GlcNAcylation sites indicates that O-GlcNAcylation at PER(S942) reduces interactions between PER and CLOCK (CLK), the key transcriptional activator of clock-controlled genes

experiments define the genetic architecture required to initiate circadian clock function in Drosophila, reveal mechanisms governing circadian activator stability that are conserved in perhaps all eukaryotes, and suggest that Clk, cyc, and cry expression is sufficient to drive clock expression in naive cells

propose that the dCLK/CYC-controlled TTFL operates differently in subsets of pacemaker neurons, which may contribute to their specific functions

ClkAR mutants showed significantly faster age-related locomotor deficits. Accelerated locomotor decline of the ClkAR mutant required expression of the PDF receptor and correlated to an apparent loss of dopaminergic neurons in the brain

Here we demonstrate that the transcription factor CLOCKWORK ORANGE (CWO) antagonizes CLK-CYC E-box binding, thus enhancing the removal of CLK-CYC from E-boxes to maintain transcriptional repression. This process requires PER, which suggests that PER-TIM and CWO cooperate to maintain a transcriptionally repressed state by removing CLK-CYC from E-boxes

these results demonstrate a key role of Clk post-transcriptional control in stabilizing circadian transcription.

Our findings suggest a novel role for clock protein phosphorylation in governing the relative strengths of entraining modalities by adjusting the dynamics of circadian gene expression.

These results demonstrate that CLK phosphorylation influences the circadian period by regulating CLK activity and progression through the feedback loop.

usp8 loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8-DN) enhances CLK/CYC transcriptional activity and alters fly locomotor activity rhythms

CLK has specific targets in different tissues, implying that important CLK partner proteins and/or mechanisms contribute to gene-specific and tissue-specific regulation

CTRIP destabilizes CLK protein in a PER-independent manner and helps degradation of phosphorylated PER and TIM in the morning

dPER(DeltaCBD) does not provoke the daily hyperphosphorylation of dCLOCK, indicating that direct interactions between dPER and dCLOCK are necessary for the dCLOCK phosphorylation

findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food

Here we examined the consequences of loss of clock function on reproductive fitness in Drosophila melanogaster with mutated period (per(0)), timeless (tim(0)), cycle (cyc(0)), and Clock (Clk(Jrk)) genes

dCLK levels are critical in mediating the direct photostimulation of locomotor activity in Drosophila.

Mouse (Murine) Clock Homolog (Mouse) (CLOCK) interaction partners

Data show that differentially expressed in chondrocytes 1 protein (DEC1) and circadian locomoter output cycles kaput protein (CLOCK) bound to E-boxes in the beta1 subunit of the Na(+)/K(+)-ATPase (ATP1B1) promoter and suppressed the expression of ATP1B1.

HNF4A strongly transrepresses the transcriptional activity of the CLOCK:BMAL1 heterodimer.

Study showed that CLOCK can interact with RANBP9 and bind with mRNAs, demonstrating that CLOCK is involved in alternative splicing in spermatogenesis. These results reveal a novel mechanism for CLOCK in spermatogenesis.

ASS1 acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1, leading to the circadian regulation of ASS1 and ureagenesis.

Human Clock Homolog (Mouse) (CLOCK) interaction partners

The present study confirmed that circadian dysfunction is associated with the risk of PD in a Chinese population at the genetic level and provided a potential genetic locus related to PD and CLOCK rs1801260 polymorphism is associated with susceptibility to Parkinson's Disease.

The CLOCK SNP may affect daytime gastric motility less than food stimulation.

Significant associations for polymorphisms in CLOCK, NPSR1 and SLC6A3 with traffic crash parameters in professional bus drivers were found.

As a novel CLOCK-dependent diurnal gene, TIMP3 inhibits the expression of inflammatory cytokines that are up-regulated by UV irradiation in human keratinocytes.

the CLOCK gene polymorphism is one of factors determining elastic properties of vascular wall

Rhythmic luciferase activity from clock gene luciferase reporter cells lines was used to test the effect of p38 MAPK inhibition on clock properties as determined using the damped sine fit and Levenberg-Marquardt algorithm.Glioma treatment with p38 MAPK inhibitors may be more effective and less toxic if administered at the appropriate time of the day.

data suggest that SNP variability in the CLOCK gene for rs6850524 and rs11932595 is associated with idiopathic recurrent spontaneous abortion in pregnancies from Slovenia and Serbia

Results indicated that inhibiting the circadian gene Clock expression can reverse the cisplatin resistance of ovarian cancer SKOV3/DDP cell lines by affecting the protein expression of drug resistance genes during which autophagy plays an important role.

Low expression of CLOCK protein is associated with kidney tumor.

Association between HCRTR2, ADH4,CLOCK gene polymorphisms and cluster headache was not significant in the present study.

No association between 3111T/C Clock gene polymorphism and complaints of patients with insomnia was detected.

Study found three gene variants (CLOCK-rs4864548, PEMT-rs936108, and GHRELIN-rs696217) that exhibited uncorrected gene-by-sleep duration interactions in relation to BMI z-scores in a cohort of New Zealand European children. However, no interactions were identified in percentage body fat differences. Notably, these interactions are evident without detectable effects on sleep duration.

These findings suggest that upregulation of the circadian gene hClock plays an important role in metastasis of colorectal cancer.

results of this study suggest that genetic variability in the ARNTL and CLOCK genes might be associated with risk for multiple sclerosis

Our results suggest that the circadian gene human Clock may play an important role in carcinogenesis by inhibiting apoptotic cell death via attenuating proapoptotic signaling

Xenopus laevis Clock Homolog (Mouse) (CLOCK) interaction partners

the second half of the photolyase homology region (PHR) of CRY is important for repression through facilitating interaction with CLOCK

CLOCK profil antigène

Antigen Summary

This gene product regulates circadian rhythm and metabolism. The protein encodes a transcription factor of the basic helix-loop-helix (bHLH) family and a DNA binding histone acetyltransferase. Polymorphisms in this gene may be associated with behavioral changes in certain populations and with obesity and metabolic syndrome. Alternative splicing results in multiple transcript variants.